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Norepinephrine Induces Lipolysis in ₁/₂/₃-Adrenoceptor Knockout Mice

Unité de Recherches sur les Obésités, Inserm UPS U586, Institut Louis Bugnard, Centre Hospitalier Universitaire de Rangueil, Toulouse, France (G.T., M.L., D.L.); Départements de Biochimie Médicale et de Physiologie Cellulaire et Métabolisme, Centre Médical Universitaire, Genève, Switzerland (M.J., J.-P.G., P.M.); and Swiss Institute of Bioinformatics, Centre Médical Universitaire, Genève, Switzerland (N.H.)

Catecholamines are major stimulants of adipose tissue metabolism. Norepinephrine and epinephrine act through three subtypes of -adrenoceptors (-AR) expressed in the adipocytes. The aim of this work was to study the mechanisms of lipid mobilization in ₁/₂/₃-AR triple-knockout (-less) mice. Glycerol and nonesterified fatty acids released from isolated adipocytes were measured as an index of lipolytic activity. There was no difference between the two genotypes for basal lipolysis and lipolytic response to corticotropin or to agents acting at the adenylyl cyclase and protein kinase A levels. The lipolytic response to norepinephrine and -AR agonists was blunted in -less mice. However, a residual low-affinity lipolytic effect was observed in the presence of catecholamines and ₃-AR agonists but not of ₁- or ₂-AR agonists. cAMP levels were increased by a -AR agonist in white and brown adipocytes of -less mice. The residual lipolytic effect was blocked by -AR antagonists. It was mediated neither by ₁- or ₂-AR nor dopaminergic, serotonergic, and histaminergic by receptors. Bioinformatic analyses do not provide evidence for a fourth -AR. We conclude that the residual lipolytic effect observed in -less mice can be attributed to an unknown Gs-protein-coupled receptor with low affinity for catecholamines.

Address correspondence to: Dr. G. Tavernier, Unité de Recherches sur les Obésités, Inserm UPS U586, Institut Louis Bugnard IFR31, CHU Rangueil, Btiment L3, BP 84225, 31432 Toulouse Cedex 4, France. E-mail: getaver{at}toulouse.inserm.fr

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